Makarova, K. S. et al. An updated evolutionary classification of CRISPR-Cas systems. Nat. Rev. Microbiol. 13, 722–736 (2015).
Mohanraju, P. et al. Diverse evolutionary roots and mechanistic variations of the CRISPR-Cas systems. Science 353, aad5147 (2016).
Barrangou, R. & Horvath, P. A decade of discovery: CRISPR functions and applications. Nat. Microbiol. 2, 17092 (2017).
Jackson, S. A. et al. CRISPR-Cas: adapting to change. Science 356, eaal5056 (2017).
Koonin, E. V., Makarova, K. S. & Zhang, F. Diversity, classification and evolution of CRISPR-Cas systems. Curr. Opin. Microbiol. 37, 67–78 (2017). This article is the latest published overview of the CRISPR–Cas diversity, with an emphasis on Class 2 systems discovered through dedicated search efforts.
Garcia-Martinez, J., Maldonado, R. D., Guzman, N. M. & Mojica, F. J. M. The CRISPR conundrum: evolve and maybe die, or survive and risk stagnation. Microb. Cell 5, 262–268 (2018).
Makarova, K. S., Wolf, Y. I. & Koonin, E. V. Classification and nomenclature of CRISPR-Cas systems: where from here? CRISPR J. https://doi.org/10.1089/crispr.2018.0033 (2018).
Faure, G., Makarova, K. S. & Koonin, E. V. CRISPR-Cas: complex functional networks and multiple roles beyond adaptive immunity. J. Mol. Biol. 431, 3–20 (2018).
Westra, E. R., Buckling, A. & Fineran, P. C. CRISPR-Cas systems: beyond adaptive immunity. Nat. Rev. Microbiol. 12, 317–326 (2014).
Shmakov, S. A., Makarova, K. S., Wolf, Y. I., Severinov, K. V. & Koonin, E. V. Systematic prediction of genes functionally linked to CRISPR-Cas systems by gene neighborhood analysis. Proc. Natl Acad. Sci. USA 115, E5307–E5316 (2018). This article presents systematic prediction and analysis of genes associated with various subsets of CRISPR–Cas systems. The results suggest substantial functional diversification of CRISPR–Cas, in particular, coupling with signal transduction, especially in type III systems.
Shah, S. A. et al. Comprehensive search for accessory proteins encoded with archaeal and bacterial type III CRISPR-cas gene cassettes reveals 39 new cas gene families. RNA Biol. https://doi.org/10.1080/15476286.2018.1483685 (2018). This paper complements Shmakov et al. (2018) by providing systematic analysis of predicted accessory proteins associated with type III CRISPR–Cas systems.
Koonin, E. V. & Makarova, K. S. Mobile genetic elements and evolution of CRISPR-Cas systems: all the way there and back. Genome Biol. Evol 9, 2812–2825 (2017).
Krupovic, M., Beguin, P. & Koonin, E. V. Casposons: mobile genetic elements that gave rise to the CRISPR-Cas adaptation machinery. Curr. Opin. Microbiol. 38, 36–43 (2017).
Krupovic, M., Makarova, K. S., Forterre, P., Prangishvili, D. & Koonin, E. V. Casposons: a new superfamily of self-synthesizing DNA transposons at the origin of prokaryotic CRISPR-Cas immunity. BMC Biol. 12, 36 (2014).
Kazazian, H. H. Jr. Mobile elements: drivers of genome evolution. Science 303, 1626–1632 (2004).
Gueguen, E., Rousseau, P., Duval-Valentin, G. & Chandler, M. The transpososome: control of transposition at the level of catalysis. Trends Microbiol. 13, 543–549 (2005).
Peters, J. E. & Craig, N. L. Tn7: smarter than we thought. Nat. Rev. Mol. Cell Biol. 2, 806–814 (2001).
Fricker, A. D. & Peters, J. E. Vulnerabilities on the lagging-strand template: opportunities for mobile elements. Annu. Rev. Genet. 48, 167–186 (2014).
Nunez, J. K., Lee, A. S., Engelman, A. & Doudna, J. A. Integrase-mediated spacer acquisition during CRISPR-Cas adaptive immunity. Nature 519, 193–198 (2015).
Hudaiberdiev, S. et al. Phylogenomics of Cas4 family nucleases. BMC Evol. Biol. 17, 232 (2017).
Shmakov, S. et al. Discovery and functional characterization of diverse class 2 CRISPR-Cas systems. Mol. Cell 60, 385–397 (2015).
Shmakov, S. et al. Diversity and evolution of class 2 CRISPR-Cas systems. Nat. Rev. Microbiol. 15, 169–182 (2017). This article presents a definitive description of the dedicated efforts on the discovery of diverse Class 2 CRISPR–Cas systems. The key finding is the identification of multiple variants assigned to subtype V-U that appear to have independently evolved from different groups of TnpB nucleases and are likely to be evolutionary intermediates on the path from TnpB to bona fide Class 2 CRISPR effectors.
Peters, J. E., Makarova, K. S., Shmakov, S. & Koonin, E. V. Recruitment of CRISPR-Cas systems by Tn7-like transposons. Proc. Natl Acad. Sci. USA 114, E7358–E7366 (2017). This article is the first description of derived CRISPR–Cas systems carried by Tn7-like transposons. A hypothetical mechanism for crRNA-guided transposition is proposed.
McDonald, N. D., Regmi, A., Morreale, D. P., Borowski, J. D. & Fidelma Boyd, E. CRISPR-Cas systems are present predominantly on mobile genetic elements in Vibrio species. BMC Genomics 20, 105 (2019).
Ozcan, A. et al. Type IV CRISPR RNA processing and effector complex formation in Aromatoleum aromaticum. Nat. Microbiol. 4, 89–96 (2019). This article presents the most thorough available characterization of the structure and biochemical activities of type IV CRISPR–Cas systems. The similarity of the effector complex structure to those of type I is demonstrated, suggesting that type IV is an extremely derived form of type I.
Maier, L. K., Dyall-Smith, M. & Marchfelder, A. The adaptive immune system of Haloferax volcanii. Life (Basel) 5, 521–537 (2015).
Seed, K. D., Lazinski, D. W., Calderwood, S. B. & Camilli, A. A bacteriophage encodes its own CRISPR/Cas adaptive response to evade host innate immunity. Nature 494, 489–491 (2013).
Naser, I. B. et al. Analysis of the CRISPR-Cas system in bacteriophages active on epidemic strains of Vibrio cholerae in Bangladesh. Sci. Rep. 7, 14880 (2017).
Roberts, A. P. & Mullany, P. Tn916-like genetic elements: a diverse group of modular mobile elements conferring antibiotic resistance. FEMS Microbiol. Rev. 35, 856–871 (2011).
Parks, A. R. et al. Transposition into replicating DNA occurs through interaction with the processivity factor. Cell 138, 685–695 (2009).
Harrington, L. B. et al. Programmed DNA destruction by miniature CRISPR-Cas14 enzymes. Science 362, 839–842 (2018). This article is an experimental validation of the interference activity of three small type V effector proteins that are closely related to TnpB and some of the subtype V-U variants described in Shmakov et al. ( Nat. Rev. Microbiol. , 2017). Preferential activity against single-stranded DNA, as opposed to double-stranded DNA, as is the case for Cas12, is demonstrated. The corresponding CRISPR–Cas type systems are now classified as subtype V-F.
Yan, W. X. et al. Functionally diverse type V CRISPR-Cas systems. Science 363, 88–91 (2019). This work complements Harrington et al. (2018) by demonstrating the activity of a distinct V-U variant (reclassified subtype V-G) that unexpectedly shows strong preference for single-stranded RNA substrates.
He, S. et al. The IS200/IS605 family and “peel and paste” single-strand transposition mechanism. Microbiol. Spectr. https://doi.org/10.1128/microbiolspec.MDNA3-0039-2014 (2015).
Chen, J. S. et al. CRISPR-Cas12a target binding unleashes indiscriminate single-stranded DNase activity. Science 360, 436–439 (2018).
Choi, K. Y., Spencer, J. M. & Craig, N. L. The Tn7 transposition regulator TnsC interacts with the transposase subunit TnsB and target selector TnsD. Proc. Natl Acad. Sci. USA 111, E2858–E2865 (2014).
Peters, J. E. Tn7. Microbiol. Spectr. https://doi.org/10.1128/microbiolspec.MDNA3-0010-2014 (2014).
Koonin, E. V. & Krupovic, M. Evolution of adaptive immunity from transposable elements combined with innate immune systems. Nat. Rev. Genet. 16, 184–192 (2015).
Nowacki, M., Shetty, K. & Landweber, L. F. RNA-mediated epigenetic programming of genome rearrangements. Annu. Rev. Genomics Hum. Genet. 12, 367–389 (2011).
Newire, E., Aydin, A., Juma, S., Enne, V. & Roberts, A. P. Identification of a type IV CRISPR-Cas system located exclusively on IncHI1B/ IncFIB plasmids in Enterobacteriaceae. Preprint at bioRxiv https://doi.org/10.1101/536375 (2019)
Carroll, K. S. et al. A conserved mechanism for sulfonucleotide reduction. PLOS Biol. 3, e250 (2005).
You, D., Wang, L., Yao, F., Zhou, X. & Deng, Z. A novel DNA modification by sulfur: DndA is a NifS-like cysteine desulfurase capable of assembling DndC as an iron-sulfur cluster protein in Streptomyces lividans. Biochemistry 46, 6126–6133 (2007).
Makarova, K. S., Wolf, Y. I. & Koonin, E. V. Comparative genomics of defense systems in archaea and bacteria. Nucleic Acids Res. 41, 4360–4377 (2013).
Simon, N. C., Aktories, K. & Barbieri, J. T. Novel bacterial ADP-ribosylating toxins: structure and function. Nat. Rev. Microbiol. 12, 599–611 (2014).
Labrie, S. J., Samson, J. E. & Moineau, S. Bacteriophage resistance mechanisms. Nat. Rev. Microbiol. 8, 317–327 (2010).
Shabbir, M. A. et al. Bacteria versus bacteriophages: parallel evolution of immune arsenals. Front. Microbiol. 7, 1292 (2016).
Villion, M. & Moineau, S. The double-edged sword of CRISPR-Cas systems. Cell Res. 23, 15–17 (2013).
Angermeyer, A., Das, M. M., Singh, D. V. & Seed, K. D. Analysis of 19 highly conserved Vibrio cholerae bacteriophages isolated from environmental and patient sources over a twelve-year period. Viruses 10, E299 (2018).
Al-Shayeb, B. et al. Clades of huge phage from across Earth’s ecosystems. Preprint at bioRxiv https://doi.org/10.1101/572362 (2019).
Hooton, S. P., Brathwaite, K. J. & Connerton, I. F. The bacteriophage carrier state of Campylobacter jejuni features changes in host non-coding RNAs and the acquisition of new host-derived CRISPR spacer sequences. Front. Microbiol. 7, 355 (2016).
Hooton, S. P. & Connerton, I. F. Campylobacter jejuni acquire new host-derived CRISPR spacers when in association with bacteriophages harboring a CRISPR-like Cas4 protein. Front. Microbiol. 5, 744 (2014).
He, F. et al. Anti-CRISPR proteins encoded by archaeal lytic viruses inhibit subtype I-D immunity. Nat. Microbiol. 3, 461–469 (2018).
Koonin, E. V. & Makarova, K. S. Anti-CRISPRs on the march. Science 362, 156–157 (2018).
Sebaihia, M. et al. The multidrug-resistant human pathogen Clostridium difficile has a highly mobile, mosaic genome. Nat. Genet. 38, 779–786 (2006).
Minot, S. et al. The human gut virome: inter-individual variation and dynamic response to diet. Genome Res. 21, 1616–1625 (2011).
Garcia-Heredia, I. et al. Reconstructing viral genomes from the environment using fosmid clones: the case of haloviruses. PLOS ONE 7, e33802 (2012).
Faure, G. et al. Comparative genomics and evolution of trans-activating RNAs in class 2 CRISPR-Cas systems. RNA Biol. https://doi.org/10.1080/15476286.2018.1493331 (2018).
Shmakov, S. A. et al. The CRISPR spacer space is dominated by sequences from species-specific mobilomes. mBio 8, e01397-17 (2017).
Anderson, E. M. et al. Systematic analysis of CRISPR-Cas9 mismatch tolerance reveals low levels of off-target activity. J. Biotechnol. 211, 56–65 (2015).
Zheng, T. et al. Profiling single-guide RNA specificity reveals a mismatch sensitive core sequence. Sci. Rep. 7, 40638 (2017).
Kleinstiver, B. P. et al. Engineered CRISPR-Cas9 nucleases with altered PAM specificities. Nature 523, 481–485 (2015).
Horvath, P. et al. Diversity, activity, and evolution of CRISPR loci in Streptococcus thermophilus. J. Bacteriol. 190, 1401–1412 (2008).
Leenay, R. T. et al. Identifying and visualizing functional PAM diversity across CRISPR-Cas systems. Mol. Cell 62, 137–147 (2016).
Zhang, Y. et al. Processing-independent CRISPR RNAs limit natural transformation in Neisseria meningitidis. Mol. Cell 50, 488–503 (2013).
Amitai, G. & Sorek, R. CRISPR-Cas adaptation: insights into the mechanism of action. Nat. Rev. Microbiol. 14, 67–76 (2016).
Pawluk, A. et al. Naturally occurring off-switches for CRISPR-Cas9. Cell 167, 1829–1838 (2016).
Pawluk, A., Davidson, A. R. & Maxwell, K. L. Anti-CRISPR: discovery, mechanism and function. Nat. Rev. Microbiol. 16, 12–17 (2018).
Maxwell, K. L. The anti-CRISPR story: a battle for survival. Mol. Cell 68, 8–14 (2017).
Varble, A., Meaden, S., Barrangou, R., Westra, E. R. & Marraffini, L. A. Recombination between phages and CRISPR-cas loci facilitates horizontal gene transfer in staphylococci. Nat. Microbiol. https://doi.org/10.1038/s41564-019-0400-2 (2019).
Koonin, E. V. & Krupovic, M. A movable defense. TheScientist https://www.the-scientist.com/features/a-movable-defense-36135 (2015).
Arndt, D. et al. PHASTER: a better, faster version of the PHAST phage search tool. Nucleic Acids Res. 44, W16–W21 (2016).